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tance may well have more to do with the lowly statusof these subspecialties within psychiatry than withthe way they are taught. At a time when

psychiatry is moving into the community it comes

as a shock to discover that in those very areas inwhich skill and knowledge will be increasinglyrequired the trainee appears most vulnerable. Manyjunior psychiatrists are receiving no formal trainingin the diagnosis and treatment of the addictions

(including alcoholism), little experience in workingwith community services, and virtually nothing inthe way of psychotherapeutic skills. In BROOK’S

group of recently appointed consultants there weresimilar gaps in training, and he comments with someirony on the fact that many consultants appeared tobe happily and confidently teaching subjects in whichthey had received next to no actual training them-selves. Research was another area for concern.

SHEPHERD 3 has pointed to the large gap between theexpanding aims of contemporary psychiatrists and theestablished knowledge required for their achievement.This fluid state of psychiatry-its peculiar suscepti-bility to social and environmental factors noted byKRAEPELIN and emphasised at Mexico by EISENBERG 4and NEKI 5-requires that those who receive a

training in it should be both aware of the limitationsof its knowledge and stimulated to advance the stateof such knowledge by research. Yet only half thetrainees in the BROOK study reportedly received anyadvice or encouragement to do research.

A disquieting trend, noted earlier by RUSSELL,6 wasfor a steady increase in the proportion of overseasdoctors staffing psychiatry and a fall in recruitmentof home-trained graduates. Apparently, British

psychiatry is failing to recruit the best from eithersource; two-fifths of the overseas graduates cameinto psychiatry as a second-best, while over a thirdcame to the U.K. with no intention of taking uppsychiatry as a career. Only a minority of the home-trained graduates possessed a higher medical quali-fication or were planning to take a higher psychiatricone, though the position has probably altered nowwith the advent of the Royal College of Psychiatrists’membership examination.The deficiencies in training highlighted in BROOK’S

report, if uncorrected, will ensure that, whateveradministrative changes may be made, the standard ofpsychiatric practice in Britain will not improve andwill almost certainly deteriorate. Calls have beenmade-and they are made again by BROoK-for moreteaching staff, for rotating programmes between

teaching and non-teaching hospitals, and for a sen-sible policy of hospital accreditation; but, in addition,serious consideration must now be given to morefundamental assessment of the whole nature of what

3. Shepherd, M. Soc. Sci. Med. 1973, 7, 95.4. Eisenberg, L. ibid. p. 97.5. Neki, J. S. ibid. p. 103.6. Russell, G. F. M. Br. J. Psychiat. 1972, 120, 333.

constitutes the practice of psychiatry, what it is thatpsychiatrists, as distinct from social workers, clinicalpsychologists, psychiatric nurses, and general practi-tioners, do and should do. Such an assessmentwas called for in the Seebohm report,7 and has beenadvocated by HILL. 8 With the passage of the years,an investigation grows more urgently; nothing inBROOK’S survey suggests the contrary.

Treatment of Paget’s Disease of BoneTHE basic pathological feature of Paget’s disease of

bone (osteitis deformans) is accelerated breakdownof bone due to excessive osteoclastic activity, fol-lowed by osteoblastic regeneration with formationof new bone which is defective and disorganised.The bone lesions may be symptomless, and in manypatients they are discovered on incidental radiologicalexamination; in others the disease may be painful andseverely disabling. The treatment of osteitis de-formans has in the past included parathyroidectomy,sodium fluoride, iodides, aspirin, and corticosteroids-all largely ineffective.9 Interest in the treatment ofosteitis deformans has been reawakened 10-12 by threeagents which more or less specifically act on bone andproduce biochemical remission.

Calcitonin, an inhibitor of osteoclastic activity,is reported not only to relieve bone pain and induceremodelling but also to diminish the cardiovascularand neurological troubles secondary to the skeletaldisturbances. 13-18 Glucagon, which potentially actsby stimulating endogenous calcitonin release, mayalso be of value.19 There are difficulties with cal-citonin. First, there is the fear that its inhibitoryaction on bone resorption may be followed by in-hibition of bone formation and, with long-termtreatment, even osteoporosis. 20 Then there is re-

sistance : HADDAD and CALDWELL 16 reported that 6 of15 patients with osteitis deformans, treated with

porcine or salmon calcitonin over periods ranging7. Report of the Committee on Local Government and Allied Personal

Social Services. H.M. Stationery Office, 1968.8. Hill, D. Psychiatry in Medicine. Nuffield Provincial Hospitals

Trust, 1969.9. Barry, H. C. Practitioner, 1973, 210, 340.

10. Lancet, 1971, i, 955.11. ibid. p. 1168.12. Br. med. J. 1973, i, 371.13. Haddad, J. G., Jr., Birge, S. J., Avioli, L. V. New Engl. J. Med.

1970, 283, 549.14. Shai, F., Baker, R. K., Wallach, S. J. clin. Invest. 1971, 50, 1927.15. Woodhouse, N. J. Y., Reiner, M., Bordier, Ph., Kalu, D. N.,

Fisher, M., Foster, G. V., Joplin, G. F., MacIntyre, I. Lancet,1971, i, 1139.

16. Haddad, J. G., Jr., Caldwell, J. G. J. clin. Invest. 1972, 51, 3133.17. Woodhouse, N. J. Y., Joplin, G. F., MacIntyre, I., Doyle, F. H.

Lancet, 1972, ii, 992.18. Woodhouse, N. J. Y., Fisher, M. T., Sigurdsson, G., Joplin, G. F.,

MacIntyre, I. Br. med. J. 1972, iv, 267.19. Condon, J. R. ibid. 1971, iv, 719.20. Bijvoet, O. L. M., van der Sluys Veer, J., Wildiers, J., Smeenk, D.

in Calcitonin 1969 (edited by S. Taylor and G. Foster); p. 351.London, 1970.

1044

from four to twenty-four months, showed signsof resistance-increased plasma-alkaline-phosphataseactivity, after an initial decrease, despite continuedand augmented hormone administration. Antibodiesto porcine and salmon calcitonin have been demon-strated in patients treated with these peptides forperiods of up to 2 years. s, 21 In the opinion of DUBEet all however, these antibodies are in such lowtitre that they may well contribute little to the

plateauing of response during long-term calcitonintreatment. 2 patients treated with synthetic humancalcitonin over 3 years had radiological bone re-

modelling with clinical and biochemical evidence ofremission and no evidence of resistance."

Mithramycin, an antibiotic produced by Strepto-myces plicatus, is a highly toxic antineoplastic drugused in the treatment of testicular malignancy; it toocan relieve pain in severe Paget’s disease ofbone.22,23Similar results have been reported with another

Streptomyces derivative, actinomycin D.24 Themechanism of action of these Streptomyces deriva-tives in Paget’s disease of bone is not clear. Thesesubstances are so toxic that they are virtually re-stricted to the elderly patient with bone pain or withincreasingly disabling complications.

Diphosphonate compounds become bound to

hydroxyapatite crystals and inhibit their growth anddissolution in vitro. SMITH, RUSSELL, and BISHOP 25produced laboratory evidence that the diphosphonateE.H.D.P. (disodium etidronate) decreased the ex-

cessive bone turnover in osteitis deformans. That

preliminary report has now been confirmed andextended by detailed work on 10 patients. 26 In 9there was a considerable decrease in the previouslyraised plasma alkaline-phosphatase activity and

hydroxyproline concentration, and also in urine totalhydroxyproline excretion, within three months ofstarting E.H.D.P. treatment. In 7 patients the valuesdecreased to normal or near-normal after up to sevenmonths. In the 1 patient who did not respondSMITH and his co-workers believe the compoundwas not properly absorbed, since the administrationof E.H.D.P. worsened the pre-existing diarrhoea.The laboratory evidence of improvement was,

however, associated with a "

striking improvement "of symptoms in only 1 patient; in 2 others there was" some improvement ". Iliac-crest specimens from

6 patients after treatment showed histological evi-dence of inactive Paget’s disease in 4 and a patchyaccumulation of osteoid in 5. SMITH et al. 26 concludethat disodium etidronate apparently reduces the

21. Dube, W. J., Goldsmith, R. S., Arnaud, S. B., Arnaud, C. D. MayoClin. Proc. 1973, 48, 43.

22. Condon, J. R., Reith, S. B. M., Nassim, J. R., Millard, F. J. C.,Hilb, A., Stainthorpe, E. M. Br. med. J. 1971, i, 421.

23. Elias, E. G., Evans, J. T. J. Bone Jt Surg. 1972, 54A, 1730.24. Fennelly, J. J., Groake, J. F. Br. med. J. 1971, i, 423.25. Smith, R., Russell, R. G. G., Bishop, M. Lancet, 1971, i, 945.26. Smith, R., Russell, R. G. G., Bishop, M., Woods, C. G., Bishop, M.

Q. Jl Med. 1973, 42, 235.

excessive resorption and remodelling of bone charac-teristic of Paget’s disease, but that, in the dose theyemployed, it also seems to impair mineralisation ofboth normal and diseased bone. HILL et al. 27 have

just reported that rats treated with E.H.D.P. developedrickets with impaired intestinal calcium transport,even when receiving large amounts of cholecalciferol.The acquired impairment of active intestinal calciumtransport was apparently due to inhibition of renalsynthesis of 1,25-dihydroxycholecalciferol 28 ; itcould not be explained, though, by a cumulativedirect inhibitory effect of E.H.D.P. on the renal

1-hydroxylase. HILL et al. 27 suggest that E.H.D.P.

acts primarily as an inhibitor of bone mineralisationand thus prevents calcium deposition in the skeleton,with a consequent hypercalcaemia which, either

directly or indirectly, through suppression of para-thyroid-hormone secretion, inhibits the renal 1-

hydroxylation of 25-hydroxycholecalciferol to the

highly intestinal-active dihydroxy metabolite. 28 Al-

though disodium etidronate undoubtedly diminishesthe excessive bone resorption characteristic of osteitisdeformans, the bone-mineralising action makes useof diphosphonates in this disorder debatable.

HEREDITARY ANGIONEUROTIC OEDEMA

WHEN a patient with a rare but well-describedcondition endures 5 operations only to receive thediagnosis " classical abdominal hysteria " 2g it is timefor memories to be refreshed. Hereditary angioneuroticoedema (H.A.E.), a condition which is inherited as anautosomal dominant,- was first recognised by Osler 30in the last century: acute, circumscribed, non-pitting,non-irritant, and painless cedema of the skin of faceor limbs is the commonest and least important mani-festation. Involvement of the mucous membrane ofthe larynx causing laryngeal oedema is much lesscommon but far more serious. (Edema of intestinalmucosa results in disabling attacks of abdominal

colic, diarrhoea, and vomiting, for which laparotomyto exclude obstruction has often been performed.Clearly laparotomy cannot always be avoided becausethe possibility of a coincidental acute surgicalemergency must always be considered. Nevertheless,a correct diagnosis made with the help of a carefulhistory and radiological investigation to show the

characteristic " picket fence " 31 or "stacked coin" 3 2

appearance of mucosal oedema will both help to

restrain the scalpel.This venerable disease has a fashionable cause: it

results from deficiency of the functional plasmainhibitor for the activated first component of comple-

27. Hill, L. F., Lumb, G. A., Mawer, E. B., Stanbury, S. W. Clin. Sci.1973, 44, 335.

28. Wills, M. R. Lancet, 1973, i, 820.29. Feller, E. J., Spiro, H. M., Katz, L. A. Gut, 1970, 11, 983.30. Osler, W. Am. J. med. Sci. 1888, 95, 363.31. Marshak, R. H., Khilnani, M., Eliasoph, J., Wolf, B. S. Am. J.

Roentg. 1967, 101, 379.32. Wiot, J. F. Semin. Roentg. 1966, 1, 219.